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Precision nutrition for children with early puberty: leveraging nutrigenomics and lipidomics analysis

為了解決Activity Diagram onl的問題，作者NGAN THI KIM NGUYEN 這樣論述：

Background: Precocious puberty (PP) is puberty occurring at an unusually early age that brings in adverse health outcomes during adolescence and adulthood. Pubertal development is a complex biological process of sexual development and is affected by genetic, nutritional, environmental, and socio-ec

onomic factors. However, the relationship between pre-pubertal intakes of energy, fat, fiber, protein levels and pubertal timing has been debated. In the genomic era, it is necessary to examine the individual response to a specific diet and how diet influences metabolic regulation in children with P

P personally. Limited evidence investigated the timing of pubertal onset by examining the interaction of nutrient intake and PP-related genetic loci. Importantly, endocrine disorders can alter lipid metabolism. The fact that puberty onset requires critical weight and body fat based on the “critical

weight hypothesis” and many lipid species have been noticed in many human obesity and metabolic syndrome studies. However, a lack of evidence works on lipidomes to propose the based-lipid biomarker and lipid metabolism in predicting PP in children.Methods: By performing a systematic review and meta-

analysis of prospective studies, we aimed to disclose the role of pre-pubertal and pubertal nutrient intake in PP development. Thereafter, we conducted a Taiwan Puberty Longitudinal Study (TPLS) in recruiting adolescents from pubertal and pediatric endocrine clinics in the Northern/Southern part of

Taiwan. The buccal samples for deoxyribonucleic acid (DNA) extraction and genotyping were collected from a total of 1404 children. We will examine the nutrient intake on the interaction with PP-related SNPs on pubertal timing using the “interaction term” of logistic regression. Also, lipidomic analy

sis deriving from 178 subjects’ plasma samples was used to identify the critical lipid biomarkers in diagnosing PP and central precocious puberty (CPP).Results: A high intake of protein, particularly animal protein, monounsaturated fatty acids (MUFAs), polyunsaturated fatty acids (PUFAs) among prepu

bertal girls were significantly associated with PP risk. We also found that SNP rs12617311, rs2090409, and rs12148769 were significantly associated with PP in children. Specifically, different genotypes interacted with such food groups and micronutrient intake. A significant interaction was observed

between intake of vegetables, fruits, fructose and menarcheal loci rs12617311 (PCL1). The rs2090409 (TMEM38B) was more likely to interact with vitamin intake. Importantly, rs12148769 (MKRN3) appeared a significant interaction with saturated FA and MUFA intake. Whist, SNP rs10980921 (ZNF483) showed

a significant interaction with total PUFAs intake. The intake of sucrose, MUFAs, and PUFAs was associated with the potential lipid-based biomarkers, such as Cer(d16:1/22:0), PI(18:2/22:1), and PI(18:2/22:2) of girls and Cer(t20:0/18:0), Cer(d18:1/16:0) and Cer(d18:1/18:1) of boys that could predict

PP and CPP onset. In addition, the lipidomic analysis proposed several candidate lipids metabolism pathways, such as sphingolipid metabolism, steroid biosynthesis, and bile acid biosynthesis for an in-depth lipid mechanism that can be linked to PP and CPP pathophysiology.Conclusion: There was an int

eraction between genetic variant, lipid metabolism, and nutrient intake that was convinced to be associated with PP and CPP development in girls and boys. Nutrient intake may be an important factor in modulating early puberty, especially the consumption of sugar, fructose, and specific saturated fat

ty acids, monounsaturated fatty acids, polyunsaturated fatty acids. Additional research is needed to determine the biological causes of individual variability in response to dietary intake. Likewise, understanding the influence of nutrigenetic interactions on dyslipidemia can aid in the development

and implementation of personalized dietary strategies to improve the PP and CPP treatment.

Association of air pollution and body composition in obstructive sleep apnea

為了解決Activity Diagram onl的問題，作者NGUYEN THANH TUNG 這樣論述：

A relationship between exposure to ambient air pollution and obstructive sleep apnea (OSA) severity was reported in epidemiological studies. Exposure to air pollution may result in increased oxidative stress, inflammation, epithelial barrier disruption, and permeability in the upper airway, which c

ould all predispose to OSA. However, there is paucity of data on the biological mechanism of this hyperpermeability. Furthermore, the overnight changes in body composition after exposure to air pollution and how they affected the severity of OSA is still unclear.To investigate the associations of bo

dy composition changes with OSA, pre- and post-sleep body composition of 1584 patients with OSA were collected. We observed that increases in limb fat deposition and visceral fat level were associated with increased OSA severity. Each increase in total fat deposition and segmental fat deposition was

associated with increased odds ratio of positional OSA. In patients with positional OSA, an increase in the fat distribution of the limbs was associated with increases in the total arousal index, especially in the non-rapid eye movement (NREM) stage.To examine the association of air pollutant expos

ure with nocturnal body composition changes and OSA, we measured pre- and post-sleep body composition of 197 subjects from a sleep center and their individual air pollution exposure (particulate matter (PM) less than 2.5 µm in aerodynamic diameter (PM2.5), ozone (O3), and nitric dioxide (NO2)). We o

bserved that exposure to air pollutants was associated with total muscle mass and leg fat percentage changes. We found an association between PM deposition in lung regions, especially in the alveolar region, and body fat accumulation in OSA. The leg fat deposition and total muscle mass changes was f

ound to be associated with the apnea-hypopnea index (AHI). These findings implied that air pollution was associated with increases in the leg fat percentage and total muscle mass changes, thus aggravating OSA severity.We then collected road dust PM2.5 from 20 cities in China and treated to human pha

ryngeal epithelial (FaDu) cells. We observed that road dust PM2.5 exposure led to declines in cell viability and increases in lactate dehydrogenase (LDH) and interleukin (IL)-6. PM2.5, especially the inorganic elemental components, led to decreases in E-cadherin and occludin and increases in EGFR an

d phosphorylated (p)-EGFR on FaDu cells, later confirmed by the knockdown of E-cadherin. The findings indicate that PM2.5 may induce the inflammation, disrupt the epithelial barrier integrity, and increase the permeability in human upper airway through the regulation of occludin, E-cadherin, EGFR, a

nd p-EGFR.Together, the air pollution-induced hyperpermeability could increase overnight fluid shift and body composition changes, thus aggravating OSA. Air pollution, particularly the PM2.5, had the potential to increase the severity of OSA through body composition changes and upper airway hyperper

meability. Our study shed light on the etiology of OSA and positional OSA. Decreasing the total fat mass and fat percentage may reduce OSA severity. Finally, measures to decrease air pollution in urban areas could be beneficial for OSA patients.